Schlaich M P, Schobel H P, Hilgers K, Schmieder R E
Department of Medicine IV/Nephrology, University of Erlangen-Nürnberg, Nürnberg, Germany.
Am J Cardiol. 2000 May 15;85(10):1199-206. doi: 10.1016/s0002-9149(00)00728-1.
Left ventricular (LV) hypertrophy is an independent risk factor for cardiovascular morbidity and mortality. Experimental data revealed that elevated circulating aldosterone is associated with increased collagen accumulation resulting in myocardial fibrosis. To analyze whether aldosterone is also associated with cardiac structural and functional changes in humans, we examined the effects of aldosterone on LV structure and function before and after suppression of aldosterone by increasing oral salt intake. The study group comprised 26 normotensive male white healthy control subjects (age 26 +/- 3 years) and 31 male white subjects (age 25 +/- 3 years) with mild essential hypertension (World Health Organization stages I to II). Two-dimensional-guided M-mode echocardiography and 24-hour ambulatory blood pressure (BP) monitoring was performed in each subject. Simultaneously, we measured 24-hour urinary sodium excretion, 24-hour urinary aldosterone, and serum aldosterone concentration at baseline and after increasing oral salt intake to suppress aldosterone secretion. In all subjects LV mass correlated with body mass index (r = 0.42, p <0.001) and both 24-hour ambulatory systolic (r = 0.28, p <0.05) and diastolic (r = 0.25, p <0.05) BP. Changes in urinary sodium excretion correlated inversely with changes in serum aldosterone concentration (r = -0.28; p <0.05). Urinary aldosterone concentration after salt loading decreased in normotensive (10.98 vs 7.44 microg/24 hours; p <0.02) but not in hypertensive (9.34 vs 10.51 microg/24 hours; p = NS) subjects. Serum and urinary aldosterone levels at baseline were not related to LV structure or function. In contrast, after increasing oral salt intake, urinary aldosterone concentration was related to LV mass (r = 0.43; p <0.01) and impaired midwall fractional fiber shortening (r = -0.33; p <0.02) in all subjects, independent of 24-hour ambulatory BP. Subgroup analysis revealed that this was significant only in hypertensive (r = 0.46; p <0.01 and r = -0.44; p <0.02, respectively) but not in normotensive (r = 0.28 and -0.16; p = NS for both, respectively) subjects. Consistently, the greater serum aldosterone remained after increasing oral salt intake, the greater was LV mass (r = 0.35; p <0.01). The latter was found in hypertensive subjects (r = 0.44; p <0.02), independent of 24-hour ambulatory BP, but not in normotensive subjects (r = 0.025; p = NS). Inadequate suppression of aldosterone in response to an increase in oral salt intake is related to LV structural and functional changes in hypertensive subjects. Thus, our results support experimental data indicating that aldosterone affects LV structure and function in humans and that this effect is BP independent.
左心室（LV）肥厚是心血管疾病发病和死亡的独立危险因素。实验数据显示，循环中醛固酮水平升高与胶原蛋白积累增加有关，进而导致心肌纤维化。为分析醛固酮是否也与人类心脏结构和功能变化相关，我们通过增加口服盐摄入量抑制醛固酮分泌，观察了醛固酮对左心室结构和功能的影响。研究组包括26名血压正常的男性白人健康对照者（年龄26±3岁）和31名患有轻度原发性高血压（世界卫生组织I至II期）的男性白人受试者（年龄25±3岁）。对每位受试者进行二维引导M型超声心动图检查和24小时动态血压（BP）监测。同时，我们在基线以及增加口服盐摄入量以抑制醛固酮分泌后，测量了24小时尿钠排泄、24小时尿醛固酮和血清醛固酮浓度。在所有受试者中，左心室质量与体重指数相关（r = 0.42，p <0.001），且与24小时动态收缩压（r = 0.28，p <0.05）和舒张压（r = 0.25，p <0.05）均相关。尿钠排泄变化与血清醛固酮浓度变化呈负相关（r = -0.28；p <0.05）。盐负荷后，血压正常受试者的尿醛固酮浓度降低（10.98 vs 7.44μg/24小时；p <0.02），而高血压受试者的尿醛固酮浓度未降低（9.34 vs 10.51μg/24小时；p =无显著性差异）。基线时的血清和尿醛固酮水平与左心室结构或功能无关。相反，增加口服盐摄入量后，尿醛固酮浓度与所有受试者的左心室质量相关（r = 0.43；p <0.01），与室壁中层部分纤维缩短受损相关（r = -0.33；p <0.02），且与24小时动态血压无关。亚组分析显示，这仅在高血压受试者中具有显著性（分别为r = 0.46；p <0.01和r = -0.44；p <0.02），而在血压正常受试者中无显著性（分别为r = 0.28和 -0.16；p均为无显著性差异）。同样，增加口服盐摄入量后血清醛固酮水平越高，左心室质量越大（r = 0.35；p <0.01）。这在高血压受试者中发现（r = 0.44；p <0.02），与24小时动态血压无关，但在血压正常受试者中未发现（r = 0.025；p =无显著性差异）。口服盐摄入量增加后醛固酮抑制不足与高血压受试者的左心室结构和功能变化相关。因此，我们的结果支持实验数据，表明醛固酮影响人类左心室结构和功能，且这种影响与血压无关。
